Morus bombycis Koidzumi extract suppresses collagen-induced arthritis by inhibiting the activation of nuclear factor-κB and activator protein-1 in mice

被引:45
作者
Kim, Hyuk Soon [1 ]
Kim, A-Ram [1 ]
Park, Hye Jin [2 ]
Park, Dong Ki [2 ]
Kim, Do Kyun [1 ]
Ko, Na Young [1 ]
Kim, Bokyung [1 ]
Choi, Dong Kug [3 ]
Won, Hyung Sik [3 ]
Shin, Wha Sup [3 ]
Kim, Young Mi [4 ]
Choi, Wahn Soo [1 ]
机构
[1] Konkuk Univ, Coll Med, Dept Immunol & Physiol, Chungju 380701, South Korea
[2] Konkuk Univ, Dept Biosci & Biotechnol, Seoul 143701, South Korea
[3] Konkuk Univ, Coll Biomed & Hlth Sci, Chungju 380701, South Korea
[4] Duksung Womens Univ, Coll Pharm, Seoul 132714, South Korea
关键词
Morus bombycis; Arthritis; Collagen-induced arthritis mice; NF-kappa B; AP-1; SIGNAL-TRANSDUCTION PATHWAYS; RHEUMATOID-ARTHRITIS; MATRIX METALLOPROTEINASES; CHEMOKINE RECEPTORS; HUMAN CHONDROCYTES; CYTOKINES; DAMAGE; AUTOIMMUNITY; INFLAMMATION; RELEASE;
D O I
10.1016/j.jep.2011.01.016
中图分类号
Q94 [植物学];
学科分类号
071001 [植物学];
摘要
Ethnopharmacological relevance: Mortis bombycis Koidzumi is widely distributed in Asia. In Korea, it has been used in traditional medicine because of its apparent anti-inflammatory, antioxidant, and hepatoprotective properties. Aim of the study: Although the extract of Morus bombycis Koidzumi (MB) has long since been used as a traditional anti-inflammatory medicine in Korea, its effect on arthritis remains unknown. We aimed to investigate the anti-arthritis activity of MB and the mechanism underlying it. Materials and methods: The anti-arthritis activity of MB was assessed by using mouse models of type II collagen-induced arthritis (CIA). The clinical arthritis index and histopathological changes were evaluated in mice. Reverse transcriptase-polymerase chain reaction (RT-PCR), electrophoretic mobility shift assay (EMSA), and other biologic approaches were used for measuring the effect of MB on arthritis and understanding the underlying mechanism. Results: MB significantly decreased the clinical arthritis index in CIA mice; this was confirmed by examining histological changes in joints. Infiltration of immune cells, synovial hyperplasia, cartilage destruction, and bone erosion in the hind paw were largely suppressed by MB. The mRNA levels of matrix metalloproteinase (MMP)-1/MMP-3, inflammatory cytokines (tumor necrosis factor (TNE)-alpha, interleukin (IL)-1 beta, IL-6), and chemokines (macrophage inflammatory protein (MIP)-1, monocyte chemoattractant protein (MCP)-1, RANTES) were significantly suppressed by MB in a dose-dependent manner. The number of osteoclasts in the hind tibia was also significantly decreased. With regard to the mechanism, MB suppressed the activation of nuclear factor (NF)-kappa B and activator protein (AP)-1 in CIA mice. Conclusions: MB produced an anti-arthritis effect in CIA mice by inhibiting the production of critical inflammatory mediators and osteoclasts through the downregulation of NF-kappa B and AP-1. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:392 / 398
页数:7
相关论文
共 38 条
[1]
Cytokines and anti-cytokine biologicals in autoimmunity: present and future [J].
Andreakos, ET ;
Foxwell, BM ;
Brennan, FM ;
Maini, RN ;
Feldmann, M .
CYTOKINE & GROWTH FACTOR REVIEWS, 2002, 13 (4-5) :299-313
[2]
Resolving conflicting signals: Cross inhibition of cytokine signaling pathways [J].
Begley, CG ;
Nicola, NA .
BLOOD, 1999, 93 (05) :1443-1447
[3]
Borzì RM, 2000, ARTHRITIS RHEUM, V43, P1734, DOI 10.1002/1529-0131(200008)43:8<1734::AID-ANR9>3.0.CO
[4]
2-B
[5]
Brahn E, 1998, J RHEUMATOL, V25, P1785
[6]
Cunnane G, 2001, ARTHRITIS RHEUM, V44, P2263, DOI 10.1002/1529-0131(200110)44:10<2263::AID-ART389>3.0.CO
[7]
2-1
[8]
Mulberry (Morus alba L.) leaves and their major flavonol quercetin 3-(6-malonylglucoside) attenuate atherosclerotic lesion development in LDL receptor-deficient mice [J].
Enkhmaa, B ;
Shiwaku, K ;
Katsube, T ;
Kitajima, K ;
Anuurad, E ;
Yamasaki, M ;
Yamane, Y .
JOURNAL OF NUTRITION, 2005, 135 (04) :729-734
[9]
Role of cytokines in rheumatoid arthritis [J].
Feldmann, M ;
Brennan, FM ;
Maini, RN .
ANNUAL REVIEW OF IMMUNOLOGY, 1996, 14 :397-440